Wasp Venom Rush Immunotherapy Induces Transient Downregulation of B Cell Surface Molecule Expression

Abstract

Background: Little is known about the involvement of B cells in venom immunotherapy (VIT). To elucidate changes in the B cell phenotype during this process, we examined the expression of several surface molecules on peripheral B cells before and during VIT. Methods: 15 venom-allergic patients with a history of systemic reactions after a wasp sting and venom-specific skin test reactivity as well as serum IgE were investigated before VIT (day 1), 1 day after reaching a maintenance dose of 100 µg (day 6) during inpatient rush VIT, and again on day 26 during continued outpatient maintenance therapy. Changes in the serum levels of total IgE, allergen-specific IgE (sIgE) and sIgG4 were measured by ELISA. Expression of several surface molecules on double-labelled B cells was studied by flow cytometry of peripheral blood mononuclear cells. Results: Levels of total IgE, sIgE and sIgG4 showed a significant increase after 26 days of VIT. On day 6, cell surface expression of HLA- II-DR, CD5, CD32 and CD54 was decreased in intensity and numbers of positive cells compared to day 1, while on day 26, expression of these molecules approached again baseline levels. Furthermore, a trend to decreased CD23 was noted on day 6. No changes were observed for CD40, CD86, CD95 and HLA-I-ABC. Conclusion: These data show that during initiation of rush VIT, B cell expression of surface molecules involved in T-B cell cooperation and antigen presentation is downmodulated. B cells may thus be additional direct or indirect targets of high-dose antigen therapy and contribute to the persistence of TH1 responses during maintenance VIT treatment.

Efficacy of birch‐pollen immunotherapy on cross‐reactive food allergy confirmed by skin tests and double‐blind food challenges

“…Whether IgG4 antibodies may be considered as blocking antibodies or just as an index of altered T cell function remains to be determined. At least the early increase is in agreement with the literature on other allergens, such as grass pollen and insect venom [33,34].…”

CD23 expression on switched memory B cells bridges T‐B cell interaction in allergic rhinitis

“…However, we failed to find any significant correlation of The inhibition of CD23 expression on total B cells has been proposed as one of the mechanisms underlying the benefit of AIT; however, previous studies did not define the contribution of distinct B-cell subsets. 43,44 In this study, we revealed that AIT only signifi- et al 21 reported that CD25 expression on B cells was selectively upregulated by Toll-like receptor agonists, suggesting that it is more relevant for infectious than for allergic condition. We found that HLA-DR was abundantly expressed on all types of B-cell subset, which is consistent with several human studies.…”

“…We further found that Tfh2 cells from AR patients had a stronger capacity to induce CD23 expression on The inhibition of CD23 expression on total B cells has been proposed as one of the mechanisms underlying the benefit of AIT; however, previous studies did not define the contribution of distinct B-cell subsets. 43,44 In this study, we revealed that AIT only significantly downregulated CD23 expression on memory B cells, with a more prominent effect on switched memory B cells, suggesting that disease modification by AIT in AR patients is mainly GC dependent and further highlighting the importance of CD23 + switched memory B cells in AR pathogenesis. How AIT decrease the CD23 expression on switched memory B cells?…”

Polymorphism R62W results in resistance of CD23 to enzymatic cleavage in cultured cells

“…Immunotherapy of allergic diseases and systemic treatment significantly reduce its expression. [12][13][14][15][16][17] In CD23-deficient transgenic mice, allergic airway hyper-responsiveness was significantly reduced in comparison to wild-type mice. Anti-CD23 antibodies also can reduce allergic airway inflammation including IgE levels and eosinophilia, and normalize allergen-stimulated airway responsiveness in wild-type sensitized mice.…”